Weissberger Gali H, Melrose Rebecca J, Narvaez Theresa A, Harwood Dylan, Mandelkern Mark A, Sultzer David L
Brain Behavior and Aging Research Center, VA Greater Los Angeles Healthcare System, Los Angeles, CA; Geriatric Research Education and Clinical Center, VA Greater Los Angeles Healthcare System, Los Angeles, CA.
Brain Behavior and Aging Research Center, VA Greater Los Angeles Healthcare System, Los Angeles, CA; Geriatric Research Education and Clinical Center, VA Greater Los Angeles Healthcare System, Los Angeles, CA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA.
Am J Geriatr Psychiatry. 2017 Jun;25(6):569-579. doi: 10.1016/j.jagp.2017.01.017. Epub 2017 Jan 31.
This study aimed to investigate the neurobiologic correlates of two distinct clusters of agitation symptoms to identify the unique biologic substrates underlying agitated behaviors.
Eighty-eight outpatients with mild to moderate Alzheimer disease (AD) were recruited from the VA Greater Los Angeles Healthcare System Geropsychiatry Outpatient Program. A cross-sectional investigation was conducted of the relationship between cerebral glucose metabolism measured via F-fluorodeoxyglucose positron emission tomography and agitated symptoms from the Neuropsychiatric Inventory (NPI) in patients with AD. Two empirically derived clusters of agitation symptoms were investigated: an Agitation factor comprising agitation/aggression and irritability/lability items of the NPI, and a Behavioral Dyscontrol factor comprising elation/euphoria, disinhibition, aberrant motor behavior, sleep, and appetite items of the NPI. Mean cerebral metabolism for patients who scored positively on each of the two factors was compared with mean cerebral metabolism for those who did not.
Patients with AD who scored positively on the Agitation factor showed reduced glucose metabolism of the right temporal, right frontal, and bilateral cingulate cortex. In contrast, the Behavioral Dyscontrol factor did not show specific neurobiologic correlates.
Symptoms encompassed within the Agitation factor have distinct neurobiologic underpinnings. The precipitants, course, and outcomes related to these symptoms may be unique from other neuropsychiatric symptoms characteristic of AD. Special attention to treatment of agitated behaviors involving anger, aggressiveness, hostility, and irritability/emotional lability is warranted, because they appear to reflect a clinically relevant symptom cluster with unique underlying neurobiologic correlates.
本研究旨在调查两种不同的激越症状群的神经生物学关联，以确定激越行为背后独特的生物学基础。
从洛杉矶退伍军人事务部大洛杉矶医疗系统老年精神病门诊项目中招募了88名轻度至中度阿尔茨海默病（AD）门诊患者。对通过F-氟脱氧葡萄糖正电子发射断层扫描测量的脑葡萄糖代谢与AD患者神经精神量表（NPI）中的激越症状之间的关系进行了横断面调查。研究了两个基于经验得出的激越症状群：一个是激越因子，包括NPI中的激越/攻击和易怒/情绪不稳定项目；另一个是行为失控因子，包括NPI中的欣快/愉悦、脱抑制、异常运动行为、睡眠和食欲项目。将在这两个因子上得分呈阳性的患者的平均脑代谢与未得分呈阳性的患者的平均脑代谢进行比较。
在激越因子上得分呈阳性的AD患者显示右侧颞叶、右侧额叶和双侧扣带回皮质的葡萄糖代谢降低。相比之下，行为失控因子未显示出特定的神经生物学关联。
激越因子所包含的症状有不同的神经生物学基础。与这些症状相关的诱因、病程和结果可能与AD的其他神经精神症状不同。对于涉及愤怒、攻击性、敌意和易怒/情绪不稳定的激越行为的治疗应给予特别关注，因为它们似乎反映了一个具有独特潜在神经生物学关联的临床相关症状群。
